Horm Metab Res 2013; 45(03): 206-212
DOI: 10.1055/s-0032-1327572
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Downregulation of Endogenous Intermedin Augmented Myocardial Injury in Rats with Ischemia/Reperfusion

X. Teng*
1   The Key Laboratory of Remodeling-related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing, China
2   Department of Physiology, Hebei Medical University, Shijiazhuang, China
3   Hebei Key Laboratory of Laboratory Animal Science, Shijiazhuang, Hebei, China
,
Y. Bian*
4   Department of Cardiology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China
,
Y. Cai
1   The Key Laboratory of Remodeling-related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing, China
,
X. Duan
5   Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
,
F. Yuan
2   Department of Physiology, Hebei Medical University, Shijiazhuang, China
,
J. Du
1   The Key Laboratory of Remodeling-related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing, China
,
W. Wu
5   Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
,
X. Wang
5   Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
,
C. Tang
1   The Key Laboratory of Remodeling-related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing, China
5   Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
,
Y. Qi
1   The Key Laboratory of Remodeling-related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing, China
5   Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Weitere Informationen

Publikationsverlauf

received12. März 2012

accepted after second revision 30. August 2012

Publikationsdatum:
27. September 2012 (online)

Abstract

Intermedin (IMD) plays an important regulatory role in cardiovascular function. We aimed to explore the protein expression of IMD and its receptors, calcitonin receptor-like receptor (CRLR) and receptor activity-modifying proteins (RAMPs), and the role of endogenous IMD in myocardial ischemia/reperfusion (I/R) injury in rats. The rat model of I/R was created by ligating cardiac left anterior descending artery. Western blot was used to determine protein expression of CRLR and RAMPs, and radioimmunoassay was used to detect IMD content. Compared with control, protein levels of CRLR and RAMPs in both ischemic and nonischemic region were upregulated at different stages of reperfusion. IMD protein content in nonischemic area myocardium also increased. However, IMD protein content in ischemic area downregulated at 3-, 6-, and 12-h reperfusion. In hypoxia/reoxygenation model of neonatal cardiomyocytes, IMD attenuated myocyte injury, and IMD receptor antagonist IMD17–47 aggravated myocyte impairment by blocking endogenous IMD. In conclusion, the downregulation of IMD at early stage of reperfusion might augment myocardium injury.

*

* These authors contributed equally to this manuscript.


 
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